A decrease in arterial contractility (i.e. maximum force per tissue cross-sectional area) has been observed in arteries from various animal models of hypertension. Since the decrease in contractility is observed in in vitro preparations which have been separated from such extrinsic contractility control, as neural and humoral factors, a change in intrinsic contractility controls is suggested. Such intrinsic controls include vessel wall structure, smooth muscle cell metabolism, and the contractile protein system. Experiments from this laboratory have examined the role played by one aspect of the contractile system, namely, the cellular content of actomyosin and indicate that the reduction in contractility that occurs in aorta from genetically hypertensive rats is not due to a loss of actomyosin. This suggests that the defect may involve an alteration in some other aspect of the force generating process of the muscle cell, a change in the structural organization of the vessel wall, or a combination of the two. The immediate objectives of this proposal are to determine which of these alterations may contribute to the observed reduction in contractility and whether they are common to different forms of hypertension; one genetic and one acquired and presumably hormonal mediated.